Clinical Correlates of Similar Pathologies in Parkinsonian Syndromes
Identifieur interne : 001C59 ( Main/Merge ); précédent : 001C58; suivant : 001C60Clinical Correlates of Similar Pathologies in Parkinsonian Syndromes
Auteurs : Yun Ju Christine Song [Australie] ; YUE HUANG [Australie] ; Glenda Margaret Halliday [Australie]Source :
- Movement disorders [ 0885-3185 ] ; 2011.
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Abstract
Background: There have been no previous studies assessing the severity of regional atrophy, cell loss and lesion densities between the overlapping conditions of Parkinson's disease (PD), progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) and relating these pathologies to different clinical features. Methods: Clinical indices and basal ganglia, brainstem, and cerebellar pathology from 43 longitudinally studied cases (PD = 8, PSP = 15, MSA = 12, controls = 8) were compared. A point-counting method was used to evaluate subregional volumes, and α-synuclein and phospho-tau immunohistochemistry was used to assess pathological inclusions and stage disease severity. Logistic regression analyses were used to identify pathological associations with clinical features. Results: All PD, PSP, and MSA cases had severe degeneration of the substantia nigra. Clinical features correlated with tissue loss and the severity of inclusion pathologies. Levodopa responsiveness and a lack of resting tremor was associated with preservation of pallidal volume, the presence of gait ataxia was associated with atrophy of the putamen, and the parkinsonian-plus phenotype with early falls and supranuclear vertical gaze abnormalities had more substantial midbrain atrophy and greater inclusion pathology in the caudate nucleus. Discussion: This is the first study to compare the severity of regional pathologies across parkinsonian conditions. The data show that tissue loss and inclusion densities in certain regions correlate with clinical indices, with regional volume changes likely to be the best indicator of clinical progression of disease.
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aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Neuroscience Research Australia and the University of New South Wales</wicri:noRegion></affiliation></author><author><name sortKey="Halliday, Glenda Margaret" sort="Halliday, Glenda Margaret" uniqKey="Halliday G" first="Glenda Margaret" last="Halliday">Glenda Margaret Halliday</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neuroscience Research Australia and the University of New South Wales</s1><s2>Randwick, New South Wales</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Neuroscience Research Australia and the University of New South Wales</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">11-0211283</idno><date when="2011">2011</date><idno type="stanalyst">PASCAL 11-0211283 INIST</idno><idno type="RBID">Pascal:11-0211283</idno><idno 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Wales</wicri:noRegion></affiliation></author><author><name sortKey="Yue Huang" sort="Yue Huang" uniqKey="Yue Huang" last="Yue Huang">YUE HUANG</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neuroscience Research Australia and the University of New South Wales</s1><s2>Randwick, New South Wales</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Neuroscience Research Australia and the University of New South Wales</wicri:noRegion></affiliation></author><author><name sortKey="Halliday, Glenda Margaret" sort="Halliday, Glenda Margaret" uniqKey="Halliday G" first="Glenda Margaret" last="Halliday">Glenda Margaret Halliday</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Neuroscience Research Australia and the University of New South Wales</s1><s2>Randwick, New South Wales</s2><s3>AUS</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Australie</country><wicri:noRegion>Neuroscience Research Australia and the University of New South Wales</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anatomic pathology</term><term>Multiple system atrophy</term><term>Nervous system diseases</term><term>Parkinson disease</term><term>Supranuclear ophthalmoplegia</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Atrophie multisystématisée</term><term>Pathologie du système nerveux</term><term>Anatomopathologie</term><term>Ophtalmoplégie supranucléaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: There have been no previous studies assessing the severity of regional atrophy, cell loss and lesion densities between the overlapping conditions of Parkinson's disease (PD), progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) and relating these pathologies to different clinical features. Methods: Clinical indices and basal ganglia, brainstem, and cerebellar pathology from 43 longitudinally studied cases (PD = 8, PSP = 15, MSA = 12, controls = 8) were compared. A point-counting method was used to evaluate subregional volumes, and α-synuclein and phospho-tau immunohistochemistry was used to assess pathological inclusions and stage disease severity. Logistic regression analyses were used to identify pathological associations with clinical features. Results: All PD, PSP, and MSA cases had severe degeneration of the substantia nigra. Clinical features correlated with tissue loss and the severity of inclusion pathologies. Levodopa responsiveness and a lack of resting tremor was associated with preservation of pallidal volume, the presence of gait ataxia was associated with atrophy of the putamen, and the parkinsonian-plus phenotype with early falls and supranuclear vertical gaze abnormalities had more substantial midbrain atrophy and greater inclusion pathology in the caudate nucleus. Discussion: This is the first study to compare the severity of regional pathologies across parkinsonian conditions. The data show that tissue loss and inclusion densities in certain regions correlate with clinical indices, with regional volume changes likely to be the best indicator of clinical progression of disease.</div></front></TEI><affiliations><list><country><li>Australie</li></country></list><tree><country name="Australie"><noRegion><name sortKey="Song, Yun Ju Christine" sort="Song, Yun Ju Christine" uniqKey="Song Y" first="Yun Ju Christine" last="Song">Yun Ju Christine Song</name></noRegion><name sortKey="Halliday, Glenda Margaret" sort="Halliday, Glenda Margaret" uniqKey="Halliday G" first="Glenda Margaret" last="Halliday">Glenda Margaret Halliday</name><name sortKey="Yue Huang" sort="Yue Huang" uniqKey="Yue Huang" last="Yue Huang">YUE HUANG</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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